ArticleNature medicine2015
Loss of BAP1 function leads to EZH2-dependent transformation.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers, 2 of them syntheses that pooled it.
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Who cites it
230 citing papers in PubMed, 2 syntheses or guidelines pooled it, 393 citations in OpenAlex.
- Primary Intrahepatic Mesothelioma: Case Series and Systematic Review of Literature.Journal of gastrointestinal cancer · 2024Pooled it
- Effect of enhancer of zeste homolog 2 mutations on the prognosis of patients with myelodysplastic syndrome: A meta-analysis.Medicine · 2020Pooled it
- Renal cell carcinoma: molecular understanding and therapeutic development.Cell death and differentiation · 2026Review
- Multidisciplinary management of meningiomas in the era of precision oncology.Nature reviews. Clinical oncology · 2026Review
- Molecular profiling and personalized medicine within EURACAN in the SPECTA Arcagen study in comparison to the France Genomic Medicine 2025 Plan in the AURAGEN platform in peritoneal mesotheliomas.Translational oncology · 2026Article
- Context-dependent synthetic lethality - an emerging precision therapeutic approach.Nature reviews. Cancer · 2026Review
- Malignant craniopharyngiomas: Institutional experience and literature review.Brain pathology (Zurich, Switzerland) · 2026Review
- BAP1 loss impairs IFN-γ signaling and enhances NK cell-mediated cytotoxicity in myeloid leukemia.Cancer immunology, immunotherapy : CII · 2026Article
- The Role of EZH2 ın Malıgnant Pleural Mesothelıoma and Beyond: Current Practıce and Future Perspectıves.Current oncology reports · 2026Review
- BRCA1-Associated Protein 1 (BAP1) in Human Cancer and its Emerging Role as a Novel Potential Therapeutic Target.Current oncology reports · 2026Review
- Splenic hamartoma in two related patients with BAP1 tumour predisposition syndrome caused by a novel germline BAP1 p.(Gly128Arg) missense variant.Familial cancer · 2026Article
- High frequency and unique subtypes of meningioma in patients with BAP1 tumor predisposition syndrome.Journal of neuro-oncology · 2026Article
- Review
- Therapeutic targeting of chromatin alterations in leukemia and solid tumors.International journal of cancer · 2026Review
- Tumor suppressor BAP1 emerges as a key regulator of metabolism and cell death in tumors.Frontiers in cell and developmental biology · 2026Review
- Molecular mechanisms of KMT2C alterations in gastrointestinal cancers: enhancer network destabilization, lineage plasticity, and clinical translation.Frontiers in immunology · 2026Review
- From biology to therapy: current standards and emerging strategies in pleural mesothelioma.Frontiers in oncology · 2026Review
- CD2 costimulation strength: A key regulator of T cell function and anti-tumor immunity that is epigenetically regulated.iScience · 2025Article
- High Frequency and Unique Subtypes of Meningioma in Patients with BAP1 Tumor Predisposition Syndrome.medRxiv : the preprint server for health sciences · 2025Article
- Clinical benefit of additional whole-exome sequencing over panel sequencing in an all-comer real-world molecular tumor board.ESMO open · 2025Article
170 more citing papers are in PubMed but not listed here.
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Authors and funding
31 authors at 4 institutions in 1 country.
Funding
Abstract
The tumor suppressors BAP1 and ASXL1 interact to form a polycomb deubiquitinase complex that removes monoubiquitin from histone H2A lysine 119 (H2AK119Ub). However, BAP1 and ASXL1 are mutated in distinct cancer types, consistent with independent roles in regulating epigenetic state and malignant transformation. Here we demonstrate that Bap1 loss in mice results in increased trimethylated histone H3 lysine 27 (H3K27me3), elevated enhancer of zeste 2 polycomb repressive complex 2 subunit (Ezh2) expression, and enhanced repression of polycomb repressive complex 2 (PRC2) targets. These findings contrast with the reduction in H3K27me3 levels seen with Asxl1 loss. Conditional deletion of Bap1 and Ezh2 in vivo abrogates the myeloid progenitor expansion induced by Bap1 loss alone. Loss of BAP1 results in a marked decrease in H4K20 monomethylation (H4K20me1). Consistent with a role for H4K20me1 in the transcriptional regulation of EZH2, expression of SETD8-the H4K20me1 methyltransferase-reduces EZH2 expression and abrogates the proliferation of BAP1-mutant cells. Furthermore, mesothelioma cells that lack BAP1 are sensitive to EZH2 pharmacologic inhibition, suggesting a novel therapeutic approach for BAP1-mutant malignancies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.